Pneumoperitoneum

Also known as: Free intraperitoneal air

Pneumoperitoneum is free gas within the peritoneal cavity. In a patient with acute abdominal pain and peritonitis, assume gastrointestinal perforation until proven otherwise.

Common surgical causes include perforated gastroduodenal ulcer, perforated diverticulitis, perforated malignancy, bowel ischaemia, traumatic perforation and anastomotic leakage.

Not all free intraperitoneal gas requires surgery. Expected postoperative gas, recent laparoscopy, peritoneal dialysis and selected thoracic or gynaecological causes can produce pneumoperitoneum without visceral perforation. Clinical context determines significance.

Perforated viscus typically produces sudden severe abdominal pain followed by localised or generalised peritoneal irritation.

Look for:

Involuntary guarding or rigidity
Increasing abdominal distension
Fever and persistent tachycardia
Reduced bowel sounds from ileus
Hypotension, oliguria or altered mentation in advanced sepsis

A patient with free air but no pain, no peritonism, normal physiology and a recent recognised benign cause should be assessed differently from a patient with rigid abdomen and shock.

CT abdomen and pelvis with IV contrast: preferred in a stable patient; confirms free intraperitoneal gas and, more importantly, attempts to identify the perforation site and associated contamination.
Plain chest or abdominal radiography may demonstrate subdiaphragmatic free gas but has substantially lower sensitivity. A negative radiograph does not exclude perforation.
Laboratory studies assess physiological consequences rather than diagnose pneumoperitoneum. Obtain full blood count, renal function, electrolytes and lactate where significant infection or hypoperfusion is suspected.

Management is determined by whether the pneumoperitoneum represents an uncontrolled perforation.

A patient with peritonitis, sepsis or haemodynamic deterioration requires immediate surgical review, resuscitation, broad spectrum antibiotics and source control.

For community acquired gastrointestinal perforation:

Ceftriaxone 2 g IV every 24 hours plus metronidazole 500 mg IV every 12 hours is reasonable in a stable lower risk patient.

For severe sepsis, major contamination or healthcare associated perforation:

Piperacillin tazobactam 4.5 g IV loading dose followed by 4.5 g IV every 8 hours by extended infusion, with renal adjustment.

Provide balanced crystalloid, correct electrolytes, insert a nasogastric tube when there is vomiting or major distension and crossmatch blood when major surgery is anticipated.

Definitive treatment depends on the source and may involve primary repair, resection with anastomosis, diversion, drainage or damage control surgery.

Do not delay theatre for additional imaging when an unstable patient has convincing generalised peritonitis and an operative source is strongly suspected.

Nonoperative observation is appropriate only when the patient is physiologically stable, has no peritonitis and there is a convincing nonsurgical explanation for the free gas. Serial examination is mandatory because deterioration changes the strategy immediately.

After adequate source control for complicated intra abdominal infection, antimicrobial therapy should generally be limited to 4 days, provided clinical recovery is appropriate.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Oesophageal Perforation

Oesophageal perforation is full thickness disruption of the oesophageal wall with leakage of oesophageal and gastric contents into the neck, mediastinum, pleural cavity or peritoneum.

Common causes are endoscopic instrumentation, dilation, surgery, spontaneous rupture, foreign bodies and trauma.

The absence of a protective serosal layer and proximity to the mediastinum allow rapid contamination, mediastinitis, pleural sepsis and shock.

Outcome is determined by location, size, underlying oesophageal disease, extent of contamination, physiological state and speed of source control.

Thoracic perforation commonly produces severe chest or upper abdominal pain, dyspnoea and systemic toxicity.

Cervical perforation may present with neck pain, dysphagia, odynophagia, cervical tenderness or subcutaneous emphysema.

Abdominal oesophageal perforation produces epigastric pain and peritonitis.

Tachycardia may be the earliest physiological abnormality. Progressive fever, respiratory distress, hypotension and organ dysfunction indicate uncontrolled contamination.

Keep strictly fasting.

Establish IV access, correct hypovolaemia and begin broad spectrum antimicrobial therapy immediately.

A practical adult regimen is:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, adjusted for renal function.

Add antifungal treatment only when there is a specific risk such as prolonged critical illness, immunosuppression, established Candida infection or another strong clinical indication. Routine empirical antifungal therapy is not required for every perforation.

Give acid suppression, for example:

Pantoprazole 40 mg IV every 12 hours.

Establish early nutrition, preferably distal enteral feeding when feasible.

A stable patient with an early, contained perforation, minimal contamination and no sepsis may be managed without open surgery provided intensive surgical, endoscopic and radiological support is immediately available. This still requires antibiotics, fasting, nutritional support and drainage of any collection.

Small iatrogenic defects, particularly below approximately 2 cm, may be closed with endoscopic clips when recognised early.

Larger defects can be treated with fully covered self expanding oesophageal stents or endoscopic vacuum therapy in selected patients. Endoscopic therapy must be combined with drainage of contaminated mediastinal or pleural spaces where necessary.

Operate urgently for:

Haemodynamic instability
Free uncontained leak
Extensive pleural or mediastinal contamination
Established sepsis not controlled by drainage
Necrotic oesophageal tissue
Failed endoscopic treatment
Underlying pathology that cannot be adequately treated conservatively

Primary repair is preferred when tissue can hold sutures. Debride devitalised margins, close the defect without tension, reinforce the repair with vascularised tissue where appropriate and provide generous external drainage.

Extensive destruction, delayed presentation with nonrepairable tissue or severe underlying oesophageal disease may require exclusion, diversion or oesophagectomy.

Delay should not be accepted simply because the perforation is more than 24 hours old. Viable repairable tissue can still be primarily repaired in selected delayed cases, but contamination control becomes increasingly important.

Pneumoperitoneum

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management